OUR GROUP. Retinoic acid (RA) increased the protein level of p16INK4a and induced p21Cip1/WAF1 protein expression; meanwhile, p27Kip1 was undetectable by immunocytochemistry in both control and RA-treated hepatic stellate cells (HSCs). However, RA had no influence on the mRNA levels of p16INK4a, p21Cip1/WAF1 or p27Kip1 as determined by in situ hybridization.
RA modulates CKIs in TGF-?1-stimulated rHSCs
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